1. Field of the Invention
The present invention relates to methods and naturaceutical formulations and substances for treating and preventing Osteoarthritis and its associated symptoms and conditions. Specifically, the present invention relates to processed Morinda citrifolia product-based methods and naturaceutical formulations and substances for treating pre-existing Osteoarthritis, as well as to Morinda citrifolia-based methods and naturaceutical formulations and substances for preventing the onset or reducing the onset potential of future or additional osteoarthritis developments. The present invention is particularly suited for treatment and prevention of Osteoarthritis as commonly experienced in mammals, and particularly humans.
2. Background of the Invention and Related Art
Osteoarthritis is a type of arthritis that is caused by the breakdown of cartilage with eventual loss of the cartilage of the joints. Cartilage is a protein substance that serves as a cushion between the bones of the joints. Osteoarthritis is also known as degenerative arthritis. Among the over 100 different types of arthritis conditions, osteoarthritis is the most common, affecting over 15 million people in the United States. Before age 45, osteoarthritis occurs more frequently in males. After age 55 years, it occurs more frequently in females. In the United States, all races appear equally affected. A higher incidence of osteoarthritis typically exists in the Japanese population, while South African blacks, East Indians and southern Chinese have lower rates.
Osteoarthritis usually affects the hands, feet, spine, and large weight-bearing joints, such as the hips and knees. Most cases of osteoarthritis have no known cause, and are called primary osteoarthritis. When the cause of the osteoarthritis is known, the condition is called secondary osteoarthritis.
Primary osteoarthritis is mostly related to aging. With aging, the water content of the cartilage increases and the protein makeup of cartilage degenerates. Repetitive use of the joints over the years irritates and inflames the cartilage, causing joint pain and swelling. Eventually, cartilage begins to degenerate by flaking or forming tiny crevasses. In advanced cases, there is a total loss of the cartilage cushion between the bones of the joints. Loss of cartilage cushion causes friction between the bones, leading to pain and limitation of joint mobility. Inflammation of the cartilage can also stimulate new bone outgrowths (spurs) that form around the joints. Osteoarthritis occasionally can be found in multiple members of the same family, implying a genetic basis for this condition.
Treating the pain associated with osteoarthritis is a common challenge for physicians. Nonsteroidal anti-inflammatory drugs (NSAIDs) have long been used to manage this disease. NSAIDs are particularly useful in treating joint pain, muscle pain, and joint swelling. There are many different types of NSAIDs, including aspirin and other salicylates. Examples include ibuprofen,(e.g., Advil®, Motrin®, Nuprin®) naproxen, sulindac, diclofenac, piroxicam, ketoprofen, diflunisal, nabumetone, etodolac, oxaprozin, and indomethacin. Popular NSAIDs include: ibuprofen, naproxen and aspirin.
The adverse side effects of NSAIDs, however, are well known and includes gastrointestinal and renal complications. In patients who take NSAIDs regularly, upper endoscopic examinations have shown a 15 to 30 percent prevalence of ulcers in the stomach or duodenum. The major side effects of NSAIDs are gastrointestinal related. For example, between 10 and 50 percent of the patients being treated with NSAIDs suffer side effects such as diarrhea, heartburn, increased abdominal pain, and upset stomach. A significant percentage of these patients also develop ulcers in the stomach and upper GI tract, which can lead to internal bleeding and other complications.
Since significant numbers of patients taking NSAIDs were suffering from an increased risk of ulceration in the stomach, researchers began investigating the mechanisms by which NSAIDs inhibit and prevent inflammation. Researchers knew that in most instances, inflammation in human tissues (and the pain associated with it) is related to the conversion of arachidonic acid (a molecule present in the majority of human body cells) into a prostaglandin in the cells of the tissue. The conversion arachidonic acid to a prostaglandin requires the presence of an enzyme known as cyclooxygenase (COX). NSAIDS were known to inhibit the COX enzyme and thereby prevent or reduce inflammation.
As researchers studied the COX inhibitory activity of NSAIDs, they discovered that there are in fact two different COX enzymes: COX-1 and COX-2. COX-1 and COX-2 are isoforms of cyclooxygenase, both of which catalyze the first two steps in the biosynthesis from arachidonic acid to the prostaglandins. The difference is that COX-1 is constitutive and COX-2 is inducible. COX-1 presents in nearly all parts of body at a constant level to produce the prostaglandins to line the stomach, maintain normal renal function, prevent platelet aggregation. On the other hand, COX-2 is normally absent from body and induced at the infected sites by those associated with inflammation such as bacterial polysaccharide and cytokines, interleukin-1, -2, and tumor necrosis factor. Once induced, COX-2 produces large amount of prostaglandins which lower the pain threshold (causes pain), raise the set point of the temperature-regulating center (causes fever), cause peripheral vasodilatation with local redness and edema formation. Therefore, the inhibition of COX-1 will lead to a series of side effects such as gastrointestinal ulceration and bleeding, renal damage, and platelet dysfunction, while the selective inhibition of COX-2 offers the advantage of inhibition of inflammation without disturbing normal body functions.
Researchers have discovered that most “first generation” NSAIDs inhibit the enzymatic activities of both COX-1 and COX-2, and do not selectively inhibit COX-2 enzyme. Therefore, when a patient takes a typical NSAID, COX-2 is inhibited and inflammation is thereby reduced, but COX-1 is also inhibited.
In order to provide relief from inflammation associated with COX-2 without losing the COX 1 enzyme, drug companies have attempted to produce drugs that selectively inhibit COX-2 without inhibiting COX-1. Selective COX-2 inhibition drugs have been developed and made available to the public for several years now. These selective COX-2 inhibition drugs were initially thought to be of special benefit to arthritis sufferers and those with chronic pain due to inflammation.
Even though selective COX-2 inhibition drugs have been reported to be a success, there are doubts about manufacturers' claims that selective COX-2 inhibition drugs are “safer” than non-selective COX inhibitors. Some of the side effects associated with non- with non-selective COX inhibitors are also found to be associated with selective COX-2 inhibition drugs. More importantly, people using selective COX-2 inhibition drugs have been shown to have four times the risk of suffering a heart attack than those taking traditional, non-selective NSAIDs.
By not inhibiting the COX-1 enzyme, selective COX-2 inhibition drugs were intended to be safer than the non-selective NSAIDs. However, there appears to be considerable risk associated with prolonged use of selective COX-2 inhibition drugs. At present, it is not known if the cause of the increased risk of heart attack associated with COX-2 inhibition is directly related to the inhibiting properties of the drug or if the increased risk of heart attack is the result of some other interaction with these particular selective COX-2 inhibition drugs. Ironically, some patients taking selective COX-2 inhibition drugs who are concerned with increased risk of heart attacks are attempting to reduce the risk by taking aspirin and other traditional non-selective NSAIDs along with the selective COX-2 inhibition drugs.
Other problems associated with the selective COX-2 inhibition drugs further complicate the ability of healthcare providers to easily and effectively treat patients suffering from inflammation. For example, in most cases selective COX-2 inhibition drugs are available by prescription only. Thus, in order to obtain these drugs, the patients are required to visit the doctor and receive a diagnosis that calls for these prescription drugs. After the visit, the patient must, of course, obtain the drugs from the pharmacy with the associated inconvenience that this process entails. Obtaining prescription drugs is much more complicated than buying over the counter pharmaceuticals or remedies and the cost of the drugs is significant.
Another disadvantage associated with selective COX-2 inhibition drugs is that they are, at present, not approved for pediatric use. Selective COX-2 inhibition drugs are unavailable to children who unfortunately may be more distressed than an adult would be by the unpleasant side effects associated with non-selective NSAIDs. Approval of pediatric selective COX-2 inhibition drugs may take several years, if such drugs are approved at all.
Other disadvantages of selective COX-2 inhibition drugs presently available also include the dangers of uncertain drug interaction for patients who are taking other medications in addition to selective COX-2 inhibition drugs. Also, pregnant women cannot take the selective COX-2 inhibition drugs during certain periods of fetal development. It has been determined that selective COX-2 inhibition drugs have teratogenic effects on fetuses. Additionally, potential harm could come to the patient if a COX 2 selective inhibitor is taken at a time when the patient is not properly hydrated.
While improvements in alternatives for treating patients with osteoarthritis have occurred in recent decades, researchers are continually attempting to obtain improved methods of treatment. Accordingly, it would be an improvement in the art to augment or even replace the treatments currently used with other treatments to provide increased results in treating osteoarthritis and its associated symptoms without negative side effects, such as gastrointestinal discomfort and other side effects. It would also be an improvement to provide a method and formulation that reduces inflammation and the pain associated with inflammation and at the same time limits the adverse side effects, such as those associated with selective COX-2 inhibition drugs of the prior art.